Prevalence and severity of disease of the protozoan parasite Toxoplasma gondii varies geographically in the wide array of hosts T. gondii infects. These facts highlight the need to discover the transmission dynamics and the genetic relationship among strains that are causing the wide spectrum of disease states identified in nature. Specifically, our research addresses the emergence and re-emergence of parasitic zoonotic diseases that have complex life-cycles with multiple routes of transmission that impact people and animals who co-exist in the same ecological niche. We seek discoveries in these areas to support the development of new diagnostic tools, discover fundamental paradigms governing virulence shifts in parasitic protozoa and ultimately develop efficacious anti-protozoal strategies to mitigate the spread of disease. This year we genotyped >80 strains isolated from an outbreak of protozoal meningoencephalitis in marine mammals off the coast of Southern California. Collectively, these strains defined a new "wild" clade of T. gondii organisms that are quite different from archetypal Type I, II and III genotypes commonly infecting people worldwide. We now refer to this new clade of strains as Type X. Ten distinct genotypes were resolved, each having a differing capacity to cause disease in otters and mice. Limited DNA sequencing identified only two alleles at all genetic loci examined, hence, the most parsimonious explanation to describe the genetic origin of these outbreak strains is that they are related progeny from a sexual cross. Reassortment in viruses is a common paradigm for the evolution of new pathogenic "Types", we believe that Toxoplasma parasites are utilizing sexual recombination (in effect, a eukaryotic version of reassortment) to evolve new pathotypes capable of occupying new "marine" niches and cause disease in susceptible animal populations such as the threatened California sea otter.